Strick, D. M.

We studied the contribution of the renal kallikrein-kinin system to short-term electrolyte and water balance during baseline and during acutely elevated renal perfusion pressure (RPP) in the anesthetized dog. Renal blood flow, glomerular filtration rate, urine flow rate, renin secretion rate, and urinary excretion of sodium, potassium, prostaglandin E2 (PGE2), and kinins were measured at baseline RPP during intrarenal infusion of 0.9% saline or the competitive bradykinin analogue [D-Arg0,Hyp3,Thi5,D-Phe7,Thi8]bradykinin (50 micrograms/min), which blocks vascular and interstitial kinin receptors. RPP was then raised above baseline (control group 25%; kinin analogue group 22%) by ligating the celiac artery, the superior mesenteric artery, and the aorta distal to the renal arteries. Renal parameters were again measured during infusion of saline or the kinin analogue. The analogue had no effect on renal hemodynamic or excretory parameters at baseline perfusion pressures. Increasing RPP significantly increased urine flow rates and urinary sodium excretion rates (control group, 43 mumol/min; kinin analogue group, 55 mumol/min) in both groups of animals. Increasing pressure also tended to decrease renin secretion rate in both groups of animals; however, neither increased pressure nor infusion of the analogue affected urinary excretion of PGE2 or kinins. The results suggest that intrarenal kinins are not powerful short-term regulators of electrolyte and water balance and that an intact kallikrein-kinin system is not necessary to induce pressure diuresis and natriuresis.

The mechanism of pressure-induced natriuresis remains controversial. To assess whether intracortical or medullary renal blood flows (RBF) change with changes in renal perfusion pressure (RPP), global and regional RBFs were measured using the dynamic spatial reconstructor, a fast computed tomography scanner, in eight anesthetized dogs (group B) within the range of RBF autoregulation (RPP of 153.5 and 114.4 mmHg). Similar measurements were obtained in seven control dogs (group A) in which RPP was not manipulated. In group B, only inner medullary perfusion decreased (from 0.84 to 0.51 ml/min per cm3 of tissue, P = 0.03) with reduction of RPP, whereas global renal, intracortical, and outer medullary perfusions remained unaltered. In group A there was no change in global or regional renal perfusion. The change in inner medullary perfusion in group B (-34.7%) was significantly different (P = 0.021) from that in group A (+27.4%). Global, cortical, and total medullary RBFs (ml/min) and volumes did not change in either group. These results suggest that with changes in RPP, the only detectable change in intrarenal perfusion occurs in the inner medulla.

Increases in renal venous pressure have been shown to consistently increase renal interstitial pressure; however, not until renal interstitial pressure is increased threefold is a natriuresis noted in normal animals. Since the intrarenal angiotensin II (Ang II) concentration has been postulated to increase with increasing renal venous pressure, the antinatriuretic action of Ang II could override the natriuretic effect of increased renal interstitial pressure. Therefore, the role of Ang II in the natriuretic response to increased renal venous pressure was examined in 10 pentobarbital-anesthetized dogs. Mean arterial pressure, renal blood flow, renal interstitial pressure, glomerular filtration rate, urinary sodium excretion, plasma renin activity, and prostaglandin E2 excretion were measured at renal venous pressures of 3, 15, and 30 mm Hg. The measurements were repeated after the administration of captopril (1 mg/kg i.v. bolus, n = 5) or [Sar1,Ile8]Ang II (50 micrograms/kg i.v. bolus + 50 micrograms/kg/hr infusion, n = 5). Under control conditions, mean arterial pressure, renal blood flow, plasma renin activity, and prostaglandin E2 excretion remained unchanged when renal venous pressure was increased. The elevations in renal venous pressure increased renal interstitial pressure from 7 +/- 2 to 12 +/- 2 and 22 +/- 4 mm Hg, while sodium excretion remained unchanged until renal venous pressure was 30 mm Hg. In the captopril-treated group, increasing renal venous pressure increased renal interstitial pressure as under control conditions; however, sodium excretion (23 +/- 4, 19 +/- 4, and 27 +/- 6 mueq/min) was not significantly increased even at the highest renal venous pressure.(ABSTRACT TRUNCATED AT 250 WORDS)